acute mesenteric ischaemia n.
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DR. N. WHEELER. ACUTE MESENTERIC ISCHAEMIA. BASIC ANATOMY. Celiac artery, SMA, and IMA supply foregut, midgut, and hindgut, respectively Celiac artery: Supplies lower esophagus, stomach, duodenum, liver, pancreas, and spleen SMA:

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basic anatomy
  • Celiac artery, SMA, and IMA supply foregut, midgut, and hindgut, respectively
  • Celiac artery:
      • Supplies lower esophagus, stomach, duodenum, liver, pancreas, and spleen
  • SMA:
    • Communication between superior and inferior pancreaticoduodenal arteries is an important anastomosis that helps to maintain bowel perfusion in atherosclerotic disease of the mesenteric vessels
    • Supplies the ileum, cecum, ascending colon, the transverse colon and communicates with the IMA.
    • Right and middle colic arteries are an important supply of blood to the marginal artery of Drummond
basic anatomy1
  • IMA:
    • Smallest mesenteric vessel
    • Supplies distal transverse, descending, sigmoid colon, rectum
    • Rectal branches offer anastomosis between visceral blood supply and the common supply
  • SMV drains the small intestine, cecum, ascending colon, transverse colon, stomach, pancreas and duodenum
  • IMV drains descending colon, sigmoid colon, rectum
  • IMV joins the splenic vein, which then joins the SMV to form the portal vein. The portal vein enters the liver
  • Insufficient blood perfusion of small bowel or colon may result from:
    • Embolic (50%) or Thrombotic arterial (25%) occlusion
    • Thrombotic venous occlusion (10%)
    • Non-occlusive processes (20%)
  • Injury severity is inversely proportional to mesenteric blood flow (number of vessels involved, systemic mean blood pressure, duration of ischemia, and collateral circulation)
  • SM vessels are more frequently involved than the IM vessels (larger diameter and better collaterals with inferior vessels)
  • Damage may range from reversible ischemia to transmural infarction with necrosis and perforation
  • Injury complicated by reactive vasospasm in SMA after initial occlusion and Arterial insufficiency causes tissue hypoxia, leading to bowel wall spasm initially(vomiting or diarrhea)
  • Mucosal sloughing may cause bleeding into the GIT
  • Minimal abdominal tenderness is present at this stage despite symptoms of intense visceral pain
  • If ischemia persists disruption of mucosal barrier occurs and bacteria, toxins, and vasoactive substances are released into the systemic circulation
  • This can cause septic shock, cardiac failure, or multi-organ failure before bowel necrosis actually occurs
  • With worsening hypoxic damage the bowel wall becomes edematous and cyanotic
  • Bowel necrosis occurs in 8-12 hours from onset of symptoms
  • Transmural necrosis leads to peritonism and indicates bad prognosis
acute mesenteric arterial embolism
  • Caused by embolism
  • Typical causes:
    • Mural thrombi - MI
    • Atrial thrombi - mitral stenosis and AF, vegetative endocarditis
    • Aortic thrombi - mycotic aneurysm, thrombi at sites of atheromatous plaques, sites of vascular aortic prosthetic grafts interposed between heart and SMA
  • Occlusion is sudden and no time to develop compensatory increase in collateral flow
  • Ischemia is more severe
  • SMA is most susceptible to emboli due to small angle and greater diameter, with IMA less commonly affected
  • CDC) Injury Center: special form of AMI due to systemic air embolism in high-energy blast injuries secondary to severe primary blast injury to the lung
acute mesenteric arterial thrombosis
  • Late complication of preexisting visceral atherosclerosis
  • Symptoms do not develop until 2 of 3 arteries are stenosed or completely blocked
  • Slow process of atherosclerotic stenosis before acute occlusion allows time for development of collateral circulation
  • Thrombus formation results in acute cessation of blood flow to GIT resulting initially in mucosal ischaemia and necrosis causing bloody stools
  • Bowel wall also becomes necrotic leading to bacterial overgrowth and bowel perforation, sepsis and death
  • Patients usually have history of atherosclerotis at other sites (eg, CAD, strokes, PVD) or other vascular disease (Aortic Aneurysms, dissections, trauma)
  • Drops in cardiac output after MI, CCF may cause AMI in pre-existing visceral atherosclerosis
  • Patients frequently present with history of chronic mesenteric ischemia and symptoms of intestinal angina before acute event
nonocclusive mesenteric ischemia
  • Precipitated by severe reduction in mesenteric perfusion secondary to arterial spasm or decreased cardiac output
  • Causes:
    • Cardiac failure
    • Shock
    • Use of potent vasopressors in critically ill patients
  • Bowel perfusion, like cerebral perfusion, is preserved in hypotension therefore NOMI represents a failure of autoregulation
  • Vasoactive drugs (eg, digitalis, cocaine, diuretics, and vasopressin) may also cause regional vasoconstriction
  • Gross pathologic arterial or venous occlusions are not observed
mesenteric venous thrombosis
  • Secondary MVT -!>80% result of processes that predispose patients to form clot in mesenteric circulation
  • Primary MVT occurs in the absence of any identifiable predisposing factor
  • Causes:
    • Malignancy
    • Blood disorders - Sickle cell disease, Protein C & S deficiency
    • Post surgery - after ligation of the splenic vein, portal vein or SMV
  • Mechanism for ischemia is a massive influx of fluid into the bowel wall and lumen, resulting in systemic hypovolemia and haemoconcentration
  • Subsequent bowel edema and decreased venous outflow impedes inflow of arterial blood and leads to bowel ischemia
  • Much younger population
mesenteric venous thrombosis1
  • Symptoms may be present longer
  • Infarction rarely observed with isolated SMV thrombosis, unless collateral flow in peripheral arcades or vasa recta is also affected
  • Fluid sequestration and bowel wall edema are more pronounced than in arterial occlusion
  • Colon rarely involved due to good callateral supply
  • Abu-Daff et al - 30-day mortality in these patients was strongly linked to colonic involvement in ischemia and to short-bowel syndrome.[26] Lack of anticoagulation also may have been a factor. The 5-year mortality, according to the investigators, was primarily related to short-bowel syndrome.
  • All-cause mortality 71% (59-93%)
  • Once bowel wall infarction has occurred the mortality is as high as 90%
  • Survivors have a high risk of rethrombosis and poor QOL due to short-gut syndrome
  • Predictors of mortality: older age, hepatic and renal impairment, metabolic acidosis, hypoxia, intramural pneumatosis, and sepsis
  • Mortality is highest for thrombotic AMI followed by NOMI, embolic AMI and venous thrombotic AMI
  • Early and aggressive diagnosis and treatment shown to reduce mortality if diagnosis made before onset of peritonitisis
  • Madrid study - described 21 patients with SMA embolus
    • Intestinal viability achieved in 100% of patients if symptoms <12 hours, 56% if <12-24 hours, and 18% if > 24 hour

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